Ubiquitin in the activation and attenuation of innate antiviral immunity

Steven M. Heaton, Natalie A. Borg, Vishva M. Dixit

Research output: Contribution to journalReview ArticleOtherpeer-review

92 Citations (Scopus)

Abstract

Viral infection activates danger signals that are transmitted via the retinoic acid-inducible gene 1-like receptor (RLR), nucleotide-binding oligomerization domain-like receptor (NLR), and Toll-like receptor (TLR) protein signaling cascades. This places host cells in an antiviral posture by up-regulating antiviral cytokines including type-I interferon (IFN-I). Ubiquitin modifications and cross-talk between proteins within these signaling cascades potentiate IFN-I expression, and inversely, a growing number of viruses are found to weaponize the ubiquitin modification system to suppress IFN-I. Here we review how host- and virus-directed ubiquitin modification of proteins in the RLR, NLR, and TLR antiviral signaling cascades modulate IFN-I expression.
Original languageEnglish
Pages (from-to)1-13
Number of pages13
JournalJournal of Experimental Medicine
Volume213
Issue number1
DOIs
Publication statusPublished - 11 Jan 2016
  • PhD Scholarship

    Steven Heaton (Recipient), 2012

    Prize: Competitive Fellowships

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